The mechanism of transformation of cells by oncogenic RNA viruses and replication of these viruses is at present unknown. In view of a number of requirements by these viruses, such as synthesis of DNA during the early phase after infection, and a continuous sensitivity to the inhibitor of DNA-dependent RNA synthesis, actinomycin D, a variety of activities of cellular nuclei are implicated. This project is directed toward a study of the different enzymes catalyzing the synthesis of DNA and RNA in normal as well as tumor virus-infected cells and the roles that the nuclear acidic and basic proteins play in the regulation of the activities of the aforementioned enzymes. The recent hypothesis of Huebner which ascribes oncogenesis to dormant viral genes in all cells can be tested by a study of "repressor" and "derepressor" or "anti- repressor" proteins in normal and virus-transformed cells. The system of murine sarcoma virus-infected mammalian cells is the model of choice. These studies are anticipated to provide useful information about the biochemical activities of nuclei in normal cells and in cells with sarcoma virus genome, expressed or unexpressed.